Alterations in biochemical pathways, such as increased flux of advanced glycation end products/receptors (AGE/RAGE), polyol pathway, protein kinase C (PKC) activation, and hexosamine pathway induced by hyperglycaemia, produce oxidative stress (Figure 2) that notably contributes to induced inflammatory intermediate production, causes the rupture of the BRB, pericytes' demise, and increased vascular permeability [42], which lead to progression to advanced DR stages and the development of vascular dysfunctions [41, 43, 44]. The gene discussed is PRRT2; the disease is Hyperglycemia.